The baroreceptor reflex buffers acute alterations in blood pressure but does not prevent the development of chronic hypertension. Several elements of the baroreflex arc may be altered in hypertension; the likely changes include a resetting and a decreased responsiveness of the baroreceptros, increased responsiveness of vascular smooth muscle, and complex changes in the central nervous system. The net effect of these abnormalities on the functional capability of the baroreflex to regulate blood pressure is unclear, largely because of limitations in previous techniques for assessing baroreflex function in intact, conscious subjects. By using a more adequate technique in the proposed study, the P.I. will derive complete stimulus-response relations for the effect of carotid sinus pressure on blood pressure and heart rate in conscious dogs before and during devlopment of perinephritic hypertension. Our recently developed surgical technique prepares the carotid sinuses for reversible isolation from the circulation; pressure within the isolated sinuses can be manipulated independently of arterial blood pressure. Normotensive and hypertensive dogs will be studied in the presence or absence of the potential buffering influence of aortic baroreceptors, and before and after pharmacologic blockade of sympathetic or parasympathetic mechanisms. Additionally, the effects on the baroreflex of chronic angiotensin-induced hypertension will be contrasted with those of acute elevation of blood pressure by norepinephrine or angiotensin. The relative roles of cardiac output and peripheral resistance in mediating baroreflex responses will be determined in normotension and chronic, angiotensin-induced hypertension. The study will (1) provide direct measurements of the extent to which autonomic dysfunction in hypertension impinges on the ability of the baroreflex to regulate blood pressure and (2) test the validity of using reflex resposes of heart rate to infer altered baroreflex sensitivity in hypertension.